Year : 2002 | Volume
: 50 | Issue : 3 | Page : 221--223
Bilateral renal artery stenosis presenting as hypertensive retinopathy and choroidopathy.
Sumeet K Malhotra, R Gupta, S Sood, L Kaur, S Kochhar
Department of Ophthalmology, Government Medical College Hospital, Sector-32, Chandigarh, India
Sumeet K Malhotra
Department of Ophthalmology, Government Medical College Hospital, Sector-32, Chandigarh
This report describes a rare case of hypertensive retinopathy with choroidopathy secondary to bilateral renal artery stenosis in a young non-pregnant female patient.
|How to cite this article:|
Malhotra SK, Gupta R, Sood S, Kaur L, Kochhar S. Bilateral renal artery stenosis presenting as hypertensive retinopathy and choroidopathy. Indian J Ophthalmol 2002;50:221-223
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Malhotra SK, Gupta R, Sood S, Kaur L, Kochhar S. Bilateral renal artery stenosis presenting as hypertensive retinopathy and choroidopathy. Indian J Ophthalmol [serial online] 2002 [cited 2021 Apr 21 ];50:221-223
Available from: https://www.ijo.in/text.asp?2002/50/3/221/14779
Ever since Liebreich in 1859 first categorized the fundus changes in malignant arterial hypertension under the designation "albuminuric retinitis", hypertensive retinopathy has widely been considered as the sole clinical entity representing all fundus changes. Over the next 130 years, a number of reports, mostly anecdotal in nature, described the occurrence of exudative retinal detachment and choroidal lesions in malignant hypertension, especially toxaemia of pregnancy or renal disease. Hayreh et al in 1986 developed an experimental model of renovascular malignant hypertension in rhesus monkeys by ligating the renal arteries and demonstrated that hypertensive choroidopathy is as important a fundus change as hypertensive retinopathy. We describe here a case of an 18-year-old girl presenting with bilateral exudative retinal deteachment and choroidopathy secondary to bilateral renal artery stenosis. To the best of our knowledge, this is the first described clinical case of hypertensive choroidopathy secondary to a bilateral renal artery stenosis and a perfect clinical parallel of the one kidney model of arterial hypertension described by Hayreh in his experiments on rhesus monkeys.
An 18-year-old female presented to us with complaints of sudden diminution of vision in both eyes, weakness of lower limbs for 2 months and headache of 7 days' duration. She gave a history of hypertension for 2 months but the cause of hypertension was undiagnosed. She underwent complete general physical and systemic examination which revealed her blood pressure (BP) at 180/160 mmHg in both arms. There was no significant variation of BP in the lower limbs. A loud S1 heart sound was noted. Neurological examination did not show any motor or sensory weakness in the lower limbs. On ocular examination, she had vision of counting fingers in both eyes. Slitlamp biomicroscopy showed sluggishly reacting pupils; 1+cells and flare in anterior chamber and 2 +cells and flare in the vitreous of both eyes. The intraocular pressure was 6 and 10mm Hg in the right and left eye respectively. On fundus examination, both eyes showed generalized arteriolar narrowing, cotton wool spots, hard exudates, flame shaped haemorrhages and disc oedema [Figure:1] and [Figure:2].
A near total serous retinal detachment was also present in both eyes. In addition, multiple, small, round, pinhead sized whitish lesions (acute focal RPE lesions or acute Elschning spots) were observed in the posterior fundus, mainly in the temporal parts as well as in the periphery. Fundus fluorescein angiography [Figure:2] showed both acute and degenerative lesions. The acute lesions stained during the late phase but the degenerative lesions showed unmasking of the choroidal fluorescence as the dye transited, and no staining during the late phase. The right eye angiogram also showed a decreased choroidal perfusion in the nasal half of macula and prominent late filling of the right superior watershed zone in the early venous phase. This was suggestive of ischaemic pathology as seen in hypertensive ocular involvement. Ultrasound B-scan showed bilateral exudative retinal detachment [Figure:3].
The patient was put on intensive anti-hypertensive therapy consisting of diuretics, α and β blockers and calcium channel blockers. Her BP fell drastically to 110/70mm Hg on addition of Tab Enalapril 5mg daily, and she had acute renal failure with oliguria and azotemia. The blood urea and creatinine levels rose to 85mg/dl and 3.6mg/dl respectively. All haematological investigations were normal. Ultrasound of abdomen showed normal kidneys and no adrenal mass was detected. Renal vascular colour doppler was carried out which showed haemodynamically significant bilateral renal artery stenosis involving origin of left renal artery and right renal artery just beyond its origin. Peak systolic and end diastolic velocities were markedly increased [Figure:4]. Echocardiography showed concentric left ventricular hypertrophy and vinyl mandellic acid (VMA) in 24 hour urine was mildly raised (9.54mg). The CT scan of brain was normal and did not show any evidence of occipital infarcts. Her BP was finally controlled slowly to 140/90mm Hg. Tablet enalapril was stopped and other drugs continued. The patient recovered vision of 6/24 in both eyes with resolution of serous retinal detachment in 2 months. The focal depigmentary changes (chronic Elschnig spots) persisted. She was referred to the nephrology department of a superspeciality hospital for renal arteriography and management of renal artery stenosis.
Retinal separation as an ocular complication of systemic hypertension with renal insufficiency is probably not as rare as the infrequent reports in the literature imply. Previous investigators have reported the occurrence of localized or bullous serous detachments of the retina in patients with toxaemia of pregnancy and accelerated or malignant hypertension. In 1982, a preliminary analysis of the findings of experimental studies by Kishi S et al suggested that fundus changes in renovascular malignant arterial hypertension consisted of three distinct entitites: hypertensive retinopathy, hypertensive choroidopathy and hypertensive optic neuropathy. The study also demonstrated that in renovascular malignant arterial hypertension, hypertensive choroidopathy is as important a fundus change as hypertensive retinopathy and that the two are independent and unrelated.
In another large laboratory study by Hayreh et al, experimental renovascular arterial hypertension was produced in 60 rhesus monkeys by one-kidney one-clip and two-kidney one-clip Goldblatt's procedures, and hypertensive fundus changes were studied in detail. In these monkeys, following marked elevation of the BP, discrete white lesions at the level of retinal pigment epithelium (RPE) and serous retinal detachment were the classic ophthalmoscopic lesions. The RPE lesions were divided into (1) acute focal lesions (due to RPE infraction) and (2) degenerative lesions which developed later. These lesions leaked fluorescein and showed staining of the damaged retinal pigment epithelium. The retinal detachment developed most commonly in the posterior pole and infrequently involved the peripheral retina. The incidence and severity of hypertensive choroidopathy was much more marked in the one-kidney model than in the two-kidney model, and the onset of arterial hypertension, after renal artery clamping was significantly earlier in the one-kidney model than in the two-kidney model. This study established that choroidal ischaemia secondary to accelerated arterial hypertension is the primary cause of hypertensive choroidopathy.
Similar findings were observed by Venecia et al in their experiments on rhesus monkeys., An interesting associated finding in their patients was variable involvement of the retinal vasculature in the form of flame-shaped haemorrhages, cotton wool spots, retinal exudates and occasional disc oedema. However, some of the patients showed almost no retinopathy except for retinal narrowing.
Our case of hypertensive choroidopathy caused by bilateral renal artery stenosis induced hypertension is a good clinical example of Hayreh's experimental one-kidney model of accelerated hypertension in rhesus monkeys. The patient developed multiple, acute focal retinal pigment epithelium (RPE) lesions and large exudative retinal detachment in the accelerated phase of hypertension. Fluorescein angiography revealed delayed filling of the choroidal vascular bed and staining of acute RPE lesions during the late phase. This patient also had changes of hypertensive retinopathy in the form of cotton wool spots, superficial haemorrhages and disc oedema. Adequate control of the BP during the early phase resulted in a rapid resolution of the detachments, disappearance of the white lesions and their replacement by variable amount of depigmentation or pigmentary clumping. At this stage fluorescein angiography should no leakage but only window defects. In patients with chronic hypertension retinal changes will usually predominate in the form of cotton wool spots, retinal exudates, retinal haemorrhages and disc oedema. Acceleration of the hypertension will lead to decompensation of the choroidal regulatory mechanism and, as in our case, the patient will show both extensive hypertensive retinopathy and choroidopathy. In conclusion, hypertensive choroidopathy is an important fundus change in hypertensive patients and can occur independently or in combination with hypertensive retinopathy.
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